Diabetic Peripheral 2

Diabetic Peripheral Neuropathy and Acrylamide - 2

See previous  “Diabetic Peripheral Neuropathy and Acrylamide” in
http://andreswhy.blogspot.com 


Dated 21/06/200

Major Money-making Opportunity.

“The end-product is path-dependant “   … AW
“You are what you eat.”
“Personalized Eating”
There are only two ways to measure the content of food :

1. Find it directly by measuring it right before you eat it . A smart fork , spoon or knife . Smart false teeth ( a new meaning for spittoon) .

Chips on a fork .

Lacking such a device , a monoclonal antibody strip should recognize the presence and concentration of a simple chemical like  acrylamide . This should be easy to make .
A personalised smart eating utensil would advise the eater of nutritional needs and no-no’s via something like blue-tooth.

This can be done now with present technology .

Market : initially , about 10% of population :huge

This is a killer app!

1. Trace the path of preparation . This is laborious , and practically impossible in a complex society .

A personal note:
I suffered increasingly for 14 years with peripheral diabetic neuropathy . When I became aware of the arguments below , I immediately (on 12/06/2006) cut out any food prepared at over 120 degrees Celsius .

The effect was dramatic. Within 2 days , a lot of the symptoms had disappeared .
( The curve is a standard exponential decreasing with time .) After 5 days I could sleep without chemical help . It is now day 10 . Glucose levels have improved , and instead of feeling hypo , I feel hungry . Still , early days .

I take daily 4x3x3 grams of Evening Primrose Oil (since 12/06/2006) , since this is the only clinically proven way of repairing peripheral neuropathy damage . Feeling is slowly returning to my feet and toes . Interestingly , there is no side-effect like in recovering from frostbite . (Tingling and burning sensations have disappeared . I still have occasional restless feet .)

The worst-case half-life of acrylamide is 8 days .
So 3-4 months should bring levels really low as long as no new acrylamide is ingested

The feeling that you have found something that actually works is indescribable .
Not only-knees up , Mother Brown , but feet-up as well !

Andre


 
1. Background:

1. Acrylamide (ACR) is a potent neuro-toxin . See http://epa.gov.iris/subst/0286.htm

2. It induces neural damage both in the Central Nervous System  (CNS) and the Peripheral Nervous System (PNS)  even at sub-chronic levels .

This has important implications for diabetes , alzheimers , etc

To quote from the experimental results in the link below :
“Thus, subchronic exposure to ACR affected the expression of death-related proteins in the CNS and PNS tissue, which indicate there is the early molecular regulatory mechanism of apoptosis in the neuropathy induced by ACR.”

Note that according to this experimental result , the CNS is somehow buffered against low continual dosages of acrylamide , but not the PNS .

The effect of acrylamide seems to change the expression of genes  bcl-2 , bax and caspase-3 to bring about apoptosis of the Scwann-cells in the myelin sheath . The result is a train crash in the axon transport system of the PNS long before effects are noted in the CNS .

Indeed , the buffering might be seen as an evolutionary work-in-progress since the invention of the use of fire + metal ( = frying) .

You might say that rats (used in the experiments) are not fire-using , but that is not correct . They do certainly eat cooked discards from human sources , and have done so for at least a million years . Given their proven speed of adaptation to poisons , propensity for gene-swapping and short gestation period ,  they are almost certainly more adept at handling acrylamide poisoning than humans . This seems to be an opportunity for some nifty forced accelerated rat-evolution and gene-science .

Since these are epigenetic expressions , the evolution can be very fast . It might even be amenable to outside intervention  in humans .

The problem is that the buffering system in the CNS is probably a stupid thing like increasing the rate of myelin-cell production . If you reduce the acrylamide by eating healthier , over-production of myelin-sheaths leads to things like Alzheimers . Eating too much acrylamide leads to neuropathy and (probably) diabetes . This is easily testable by feeding rats with Alzheimers acrylamide in controlled dosages . Has this been done ?

See link :
http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3048&uid=16242231&db=pubmed&url=http://linkinghub.elsevier.com/retrieve/pii/S0300-483X(05)00385-9

2. Acrylamide formation.

“The end-product is path-dependant “   … AW

The standard theory of formation of acrylamides involves a temperature over 120 degrees Celsius somewhere in the process .

So it was a shock when the FDA found very high concentrations of acrylamide in canned black olives and bottled prune juice . At first glance , the temperatures of canning and bottling (127 – 140 celsius) does not seem to high enough .
But it seems that both are washed in lye . And in the US the lye is laced by up to 0.2% of acrylamide ( see FDA regulations below) .

(It was extraordinarily difficult to get any information about processes and intermediate materials , mainly because the present model is path-independent . Potent sub-chronic intermediate chemicals are not taken into account at all .)

Black Ripe Canned Olives:Most olives in California are grown to supply canneries with green fruit to produce this canned dark olive we see on pizzas and in tacos and in every grocery store. The dark color is not a result of ripeness but of a process of lye curing and oxidizing the olive. The cured olive is pasteurized and canned in a light salt brine. If you open one of these cans and a small film is floating on top of the brine, it is most likely oil from the olive that has floated to the top. Many cans of olives are needlessly thrown out for this reason.

FDA regulations .
These were formulated before the extent of acrylamide became known . Due to bureaucratic inertia , they have not changed . So some foods are still prepared using dangerous levels of acrylamide .

AA=AcrylAmide
PAA=PolyAcrylAmide
U.S FDA (1998) regulates AA as an indirect food additive, a component of food-contact surfaces for single and repeated use. PAA has been approved for various applications. MPC in food contact PAA solutions: 0.02% (1990); MPC for PAA food additive: 0.05 to 0.2%. 
US FDA has established regulations for use of AA: It can be used (l) in washing or to assist in the peeling of fruits and vegetables using lye if the concentration does not exceed 10 mg/l in the wash water and if no more than 0.2% AA is present; (2) in adhesives as a component (monomer) of articles intended for use in packaging, transporting, or holding food in accordance with the conditions prescribed in 21 CFR part 175.105; as (3) a component (monomer) of the uncoated or coated food-contact surface of paper and paperboard intended for use in producing, manufacturing, packaging, processing, preparing, treating, packing, transporting, or holding dry food in accordance with the conditions prescribed in 21 CFR part 176.180; (4) as a monomer in the manufacture of semirigid and rigid acrylic and modified acrylic plastics in the manufacture of articles intended for use in contact with food in accordance with the conditions prescribed in 21 CFR part 177.1010. (5) AA-sodium acrylate resins can be used as boiler water additives in the preparation of articles that will be in contact with food, if the water contains not more than 0.05% by weight of AA; (6) PAA can be used as a film former in the imprinting of soft-shell gelatin capsules if no more than 0.2% of the monomer is present; (7) homopolymers and copolymers of AA may be safely used as food packaging adhesives, providing the amount used does not exceed that "reasonably required to accomplish the intended effect"; (8) AA-acrylic acid resins may be safely used as components in the production of paper or paperboard used for packaging food, providing the resin contains less than 0.2% residual monomer and that the resin does not exceed 2.0% by weight of the paper or paperboard

From another site : an interesting snippet for rats :
From PMID: 2539170 [PubMed - indexed for MEDLINE]

Quote :
“This study supports the concept that acrylamide neuropathy worsens with moderate intensity of running activities for a prolonged period and that recovery may occur if vigorous exercise is avoided.”

Another feather in the scale of acrylamide vs hyperglucose : vigorous exercise will decrease glucose faster than acrylamide.


3. This is a simple , but very clear experiment illustrating the links between acrylamide and diabetes .

The implications of this article are enormous . Is it true ? Has any other comparable experiments been done ?

The inference is that , taken together with the sub-chronic data about acrylamide , the chicken-and-egg situation between acrylamide and diabetes resolves to a “acrylamide first” picture .

In other words , the diabetic feedback condition is kicked off by prolonged sub-chronic acrylamide poisoning . While  acrylamide does not accumulate in tissue or blood  , the damage it does is repaired at a slower rate than ingestion . Diabetes seems to be an attempt of the body to get nutrients to nerve-extremities that have been cut off from supplies by axon-transport diminishment .

Instead of a disease , diabetes (at least at the start ) seems to be an attempt at a cure .

Curing it :
1.Cut all acrylamide ingestion . This means any food prepared at over 120 degrees Celsius or containing very small amounts ( micrograms ) of acrylamides (like  canned olives , bottled prune juice , anything washed by lye)
2. Do not exercise vigorously until 8 days have passed since cutting all acrylamide ingestion .
3. Type II diabetes should taper off . (This needs to be proven.)
4. Take high concentrations of Evening Primrose Oil: the only clinically proven substance to reverse peripheral neuropathy . Obviously , it will only work well if intake of acrylamide is sharply reduced .



Attenuation of acrylamide-induced neurotoxicity in diabetic rats.Al Deeb S, Al Moutaery K, Arshaduddin M, Biary N, Tariq M.Neuroscience Research Group, Armed Forces Hospital, P.O. Box 7897 (W-912), Riyadh, Saudi Arabia.In recent years, an increasing number of cases of neuropathy have been reported as a result of accidental or occupational exposure to chemicals. Acrylamide (Acr), a widely used industrial chemical, is known to produce peripheral neuropathy that resembles diabetic neuropathy in many ways. However, the interaction between diabetes and Acr has not been studied. The present study was undertaken to examine the effect of streptozotocin (STZ)-induced diabetes on Acr-induced neurotoxicity in rats. Male Sprague-Dawley rats weighing 300 +/- 10 g were divided into four groups of 10 animals each. The rats in group 1 served as control, and received normal saline. The animals in group 2 were given Acr dissolved in physiological saline (50 mg/kg IP 3 days/week) for 2 weeks. The rats in group 3 and 4 were made diabetic by administering a single IP injection of STZ (50 mg/kg). The animals in group 3 served as diabetic control, whereas the rats in group 4 received Acr in the same dose regimen as in group 2, a week after induction of diabetes. Neurobehavioral responses including foot print length, hind limb function, landing foot splay, and the ability to stay on an inclined plane were assessed 48 h after the last dose of Acr followed by electrophysiological measurements. The animals were then sacrificed, and sciatic nerves were collected for biochemical analysis. The results of this study clearly showed a significant deterioration of neurobehavioral and electrophysiological responses in Acr-treated rats. Although no significant change in these parameters was observed in the diabetic (only) group, Acr-induced functional deficiency was significantly reduced in diabetic animals. However, the difference in electrophysiological response in Acr-treated diabetic and nondiabetic rats was not found to be statistically significant (p 0.05). The precise mechanism by which Acr induced neurobehavioral toxicity is reduced in diabetic animals warrants further investigations.PMID: 10758354 [PubMed - indexed for MEDLINE]



Happy eating
Andre